Triglyceride is transported in plasma mainly by very low density lipoproteins (VLDL) and chylomicrons. VLDL and chylomicron hydrolysis is facilitated by the enzyme extrahepatic lipoprotein lipase. A polypeptide, apolipoprotein CII, which is found in chylomicrons, VLDL, and high density lipoporoteins (HDL) is necessary for the activation of lipoprotein lipase and for the metabolic clearance of circulating VLDL triglyceride. In hypertriglyceridemic VLDL, there is an absolute deficiency of apoCII and inhibition in its LPL activating potency. Apolipoprotein CIII inhibits activation of lipoproteiin lipase in vitro. Development of accurate, precise sensitive and specific radioimmunoassays for both apolipoprotein CII and CIII would allow evaluation of quantitative or qualitative defects in these activator and inactivator peptides in patients with familial and acquired hypertriglyceridemia. A better understanding of the in vitro interaction of apoCII and CIII between VLDL and HDL would also allow for approaches to accelerated VLDL catabolism and would allow preliminary studies focused on methods designed to increase VLDL apoCII levels and its LPL activator property. Ultimately, radioimmunoassay techniques for measurement of apoCII and CIII will allow a better understanding of their interaction with lipoprotein lipase in familial and acquired hypertriglyceridemia.